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Splenic infarction

Splenic infarction is the ischemic necrosis of splenic tissue resulting from compromised blood flow, often due to arterial or venous occlusion, which can affect a segmental or the entire spleen.^[1] This condition typically manifests as an acute medical issue, presenting with left upper quadrant abdominal pain in approximately 50% of cases, and is frequently associated with underlying hematologic disorders, thromboembolic events, or trauma.^[1] While rare, its incidence appears to be increasing with the widespread use of advanced imaging modalities that detect incidental cases.^[1] The etiology of splenic infarction is diverse, encompassing thromboembolic diseases such as atrial fibrillation or endocarditis, hematologic malignancies like leukemia and lymphoma, and hypercoagulable states including sickle cell disease.^[1] Other causes include blunt abdominal trauma, pancreatic pathology that compresses splenic vessels, and infectious processes leading to vascular occlusion.^[1] In patients under 40 years of age, hematologic illnesses predominate, whereas those over 40 are more likely to experience thromboembolic origins.^[1] The spleen's unique vascular supply from the splenic artery and short gastric vessels renders it susceptible to infarction, particularly in the context of splenomegaly, which heightens the risk of vascular compromise.^[1] Clinically, patients often report sudden-onset left-sided abdominal pain, with additional findings such as splenomegaly in 32% of cases, fever exceeding 38°C in 36%, and leukocytosis above 12,000 cells/μL in 56%.^[1] Elevated lactate dehydrogenase (LDH) levels are observed in 71% of affected individuals, though these markers lack specificity for diagnosis.^[1] Up to 31% of cases may present without localized physical signs, complicating initial assessment.^[1] Diagnosis is primarily confirmed through contrast-enhanced computed tomography (CT), which reveals characteristic wedge-shaped hypodense lesions indicative of infarction; ultrasonography serves as an alternative, showing hypoechoic areas.^[1] Management focuses on supportive care, including analgesia, hydration, and monitoring for complications, with most uncomplicated cases resolving within 7 to 14 days.^[1] In patients with sickle cell disease, prompt correction of hypoxia or acidosis is essential to prevent progression.^[1] Suspected infectious etiologies warrant broad-spectrum antibiotics, while severe complications such as abscess formation, splenic rupture, or hemorrhage may necessitate surgical intervention, including splenectomy.^[1] Post-treatment, vaccination against encapsulated organisms is recommended for asplenic patients to mitigate infection risks.^[1]

Overview and Epidemiology

Definition

Splenic infarction refers to the occlusion of the splenic vascular supply, resulting in parenchymal ischemia and subsequent tissue necrosis of the spleen. This condition arises from arterial or venous compromise, leading to inadequate blood flow and oxygen delivery to splenic tissue. It can manifest as segmental infarction, affecting only a portion of the organ, or global infarction, involving the entire spleen.^[1] The spleen is a fist-sized organ situated in the left upper quadrant of the abdomen, beneath the diaphragm and behind the stomach. It serves critical physiological roles, including filtering blood to remove old or damaged red blood cells, storing platelets and white blood cells, and contributing to the immune response by producing lymphocytes and antibodies that combat infections, particularly against encapsulated bacteria.^[2]^[3]^[4] Splenic infarction is classified into acute and chronic types based on onset and progression. Acute infarction presents with sudden vascular occlusion, often causing rapid tissue death, whereas chronic infarction develops gradually through repeated ischemic events, commonly in hematologic disorders such as sickle cell disease, which can culminate in progressive fibrosis and functional autosplenectomy by adulthood.^[1]^[5]

Epidemiology

Splenic infarction is a rare cause of acute abdominal pain, with an estimated incidence of 8.9 cases per 100,000 person-years among patients diagnosed via CT scan in emergency department settings.^[6] The condition has an annual incidence of approximately 1 in 100,000 in the general population.^[7] Demographic patterns show a mean age at diagnosis of around 52 years, though medians vary across studies from 52 to 71 years, with a slight male predominance in some cohorts (e.g., 60%).^[1]^[6] It occurs more frequently in patients under 40 years with underlying hematologic illnesses, such as sickle cell disease where repeated infarctions commonly lead to functional asplenia by early adulthood, accounting for a substantial proportion of cases in this age group; in contrast, patients over 40 years are more likely to have thromboembolic etiologies.^[1] Diagnosis rates have increased due to the widespread use of advanced imaging modalities like CT and ultrasound, along with trends favoring nonoperative management of splenic injuries.^[1]^[8] The condition shows higher prevalence in specific populations, including up to 19% of patients with left-sided infective endocarditis undergoing valvular surgery.^[9] Cases associated with COVID-19-induced coagulopathy have also been reported, particularly following the 2020 pandemic onset.^[7] Global variations are notable, with higher reporting in regions of elevated sickle cell disease prevalence, such as sub-Saharan Africa, where about two-thirds of the world's sickle cell population resides and splenic complications are more common.^[10]

Etiology and Pathophysiology

Causes

Splenic infarction results from occlusion of the splenic vasculature, leading to ischemia and necrosis of splenic tissue. The etiology is diverse, encompassing hematologic disorders, thromboembolic events, infections, iatrogenic interventions, and other conditions. In patients under 40 years of age, hematologic diseases predominate, while thromboembolic causes are more common in those over 40.^[1] Hematologic disorders account for a significant proportion of cases, often through infiltration causing vascular congestion or splenomegaly that increases oxygen demand and predisposes to infarction. Common examples include sickle cell disease, where red blood cell sickling under hypoxia leads to microvascular occlusion; leukemia and lymphoma, which infiltrate the splenic parenchyma; and myeloproliferative neoplasms such as myelofibrosis and chronic myeloid leukemia, with infarction rates reported up to 72% in myelofibrosis and 50% in chronic myeloid leukemia.^[1]^[11]^[11] Thromboembolic events represent another major category, typically originating from cardiac sources and obstructing larger splenic vessels. These include emboli from atrial fibrillation, infective endocarditis (with splenic infarction occurring in up to 19% of left-sided cases), and nonbacterial thrombotic endocarditis such as Libman-Sacks endocarditis associated with systemic lupus erythematosus. Hypercoagulable states, including antiphospholipid syndrome and deficiencies in protein C or S, also contribute by promoting thrombus formation.^[1]^[11]^[11] Infectious causes are less frequent but well-documented, particularly in conditions that induce splenic sequestration or vascular inflammation. Examples include malaria and babesiosis, which cause intraerythrocytic parasites leading to microvascular obstruction, and infectious mononucleosis due to Epstein-Barr virus, which can result in splenomegaly and secondary infarction.^[12] Iatrogenic causes arise from therapeutic interventions, such as splenic artery embolization performed for hypersplenism or trauma management, which intentionally or inadvertently compromises blood flow.^[1] Other etiologies include blunt abdominal trauma, which disrupts splenic vessels through direct injury; pancreatic disorders like acute pancreatitis, causing extrinsic compression or thrombosis of the splenic vein; and portal hypertension, leading to venous congestion. Emerging associations include COVID-19 infection, where hypercoagulability and endothelial dysfunction have been linked to splenic thrombosis in multiple case reports from 2020 onward.^[1]^[11]^[13]

Pathophysiology

Splenic infarction primarily arises from arterial or venous occlusion, including thrombosis, embolism, or vasospasm, which compromises blood flow to the splenic parenchyma, leading to ischemia and subsequent tissue necrosis.^[1] The splenic artery supplies the organ via end-arterial branches, making it particularly vulnerable to segmental occlusion; ischemia develops rapidly due to the spleen's high metabolic demand, with irreversible necrosis occurring after prolonged deprivation of oxygen and nutrients, typically within hours of complete occlusion.^[11] Venous occlusion, such as from thrombosis in the splenic vein, can cause outflow obstruction, resulting in congestion, edema, and ischemia even without arterial compromise.^[11] In sickle cell disease, the pathophysiology involves hypoxia-induced polymerization of deoxygenated hemoglobin S (HbS), which distorts erythrocytes into rigid sickle shapes, promoting microvascular occlusion within the spleen's low-oxygen environment.^[14] This sickling obstructs splenic sinusoids and small vessels, causing recurrent ischemic episodes that culminate in progressive fibrosis, scarring, and eventual functional asplenia, often by early adulthood in homozygous cases.^[11] Splenomegaly exacerbates this vulnerability; an enlarged spleen, as seen in hematologic malignancies like leukemia or myelofibrosis, increases oxygen demand and intrasplenic pressure, rendering even partial vascular compromise sufficient to precipitate infarction.^[1] In cases of wandering spleen, torsion of the splenic pedicle leads to venous outflow obstruction, causing splenic congestion, ischemia, and infarction due to the mechanical twisting of vascular structures.^[11] Following infarction, an inflammatory response ensues, characterized by local cytokine release and leukocyte infiltration, which can contribute to further tissue damage; partial restoration of blood flow may trigger reperfusion injury through oxidative stress and additional inflammation.^[1] The resulting necrotic areas typically manifest as wedge-shaped peripheral infarcts, reflecting the end-arterial distribution of splenic blood supply, with the apex directed toward the hilum and the base at the capsule.^[11]

Clinical Presentation

Symptoms

The primary symptom of splenic infarction is sudden onset of severe left upper quadrant abdominal pain, reported in up to 70% of cases.^[15] This pain may radiate to the left shoulder, known as Kehr's sign, due to irritation of the diaphragm.^[15] It can be constant or colicky and is often the most prominent patient-reported manifestation.^[1] Associated symptoms include nausea and vomiting in approximately 32% of patients, as well as fever exceeding 38°C in about 36%.^[1] In infectious etiologies, fever may be more pronounced, reflecting the systemic response.^[15] Up to 50% of cases, especially those involving small or chronic infarcts in patients with hematologic disorders, may be asymptomatic and discovered incidentally.^[16] Pain typically peaks within 24-48 hours and resolves over 7-14 days with conservative management.^[16] Symptom variations depend on the underlying cause; in traumatic cases, pain is immediate and severe, while embolic infarctions often present with abrupt onset.^[15]

Physical Findings

Physical examination in splenic infarction often reveals findings localized to the abdomen, though systemic signs may also be present depending on the underlying etiology. During abdominal assessment, left upper quadrant tenderness is noted in approximately 36% of cases, sometimes accompanied by guarding or rebound tenderness indicative of peritoneal irritation.^[17] Splenomegaly may be palpable in about 32% of patients, particularly those with hematologic disorders such as sickle cell disease or myeloproliferative neoplasms, where the enlarged spleen predisposes to infarction.^[1] Systemic manifestations can include fever in 36% of patients, often exceeding 38°C.^[17] Tachycardia may occur, reflecting the inflammatory response or hypovolemia.^[18] Notably, up to 31% of patients exhibit no localized physical signs referable to the spleen, which can contribute to diagnostic delays as the condition mimics other abdominal pathologies.^[17] In instances of massive infarction involving a significant portion of the splenic parenchyma, complications such as subcapsular hematoma or rupture may lead to hypotension or shock, presenting with signs of hemodynamic instability including profound tachycardia and reduced perfusion.^[19] Rare physical findings include a splenic friction rub, described historically by William Osler as a peritoneal rub over the left upper quadrant due to fibrinous inflammation on the splenic surface.^[20]

Diagnosis

Laboratory Evaluation

Laboratory evaluation in splenic infarction typically includes routine blood tests to assess for inflammation, hemolysis, and tissue damage, though no single laboratory finding is diagnostic. Common abnormalities include leukocytosis, with white blood cell counts exceeding 12,000/μL in approximately 56% of cases, often reflecting an inflammatory response to infarction.^[20] Elevated lactate dehydrogenase (LDH) levels are observed in about 71% of patients, attributable to splenic tissue necrosis releasing intracellular enzymes.^[20] Mild anemia may also be present, potentially due to underlying hematologic conditions or minor hemolysis associated with the infarct.^[21] Serum amylase is usually normal or only mildly elevated, helping to distinguish splenic infarction from acute pancreatitis.^[22] Specific tests are directed toward identifying underlying etiologies, particularly in cases suggestive of thromboembolic or hematologic disorders. Coagulation studies, including D-dimer levels, are often elevated in the setting of thromboembolism and warrant further evaluation for hypercoagulable states.^[7] A peripheral blood smear may reveal sickle cells in patients with sickle cell disease or blasts in those with leukemia, guiding targeted workup.^[1] Inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are commonly elevated, indicating systemic inflammation secondary to the infarct.^[23] If infectious endocarditis or sepsis is suspected as a cause, blood cultures should be obtained to identify potential pathogens.^[1] Laboratory findings lack specificity for splenic infarction and are primarily used to support diagnosis and direct investigation into precipitating factors, such as measuring troponin levels to evaluate for a cardiac embolic source.^[1] These results may correlate with infarct size observed on imaging, with more pronounced elevations in LDH and leukocytosis associated with larger infarcts.^[20] In patients with sickle cell disease, a high reticulocyte count is typically seen during vaso-occlusive crises involving splenic infarction, reflecting compensatory erythropoiesis amid hemolysis.^[24]

Imaging Studies

Contrast-enhanced computed tomography (CT) of the abdomen is the gold standard imaging modality for diagnosing splenic infarction, with high sensitivity exceeding 90% once the infarct is established.^[16] It typically reveals wedge-shaped, peripheral hypodense lesions with rim enhancement in partial infarcts, while global infarction appears as a non-enhancing spleen.^[25] The portal venous phase is preferred for optimal visualization, as arterial phase enhancement can be heterogeneous and obscure findings.^[16] Ultrasound serves as an initial bedside tool, particularly in hemodynamically unstable patients or during pregnancy, where it demonstrates hypoechoic areas corresponding to infarcted tissue.^[26] Color Doppler ultrasound can assess vascular flow, showing diminished or absent perfusion in affected regions, though overall sensitivity is limited at approximately 18%.^[26] A characteristic "bright band sign"—echogenic linear bands at the infarct periphery—may aid diagnosis in select cases.^[16] Magnetic resonance imaging (MRI) is reserved for equivocal cases or when CT is contraindicated, providing detailed characterization with T2-weighted hyperintense signals in infarcted areas and hypoenhancement on gadolinium-enhanced sequences.^[25] It excels in delineating tissue viability and complications like hemorrhage.^[26] Nuclear scintigraphy, such as technetium-99m sulfur colloid scanning, is rarely employed but useful for functional assessment in scenarios like congestive splenomegaly, where it highlights areas of absent splenic uptake.^[27] Imaging findings evolve over time: acute infarcts appear hypodense or hypoechoic without enhancement, subacute lesions develop a peripheral enhancing rim due to granulation tissue, and chronic stages show splenic atrophy, volume loss, or cystic changes from liquefaction.^[25] In traumatic settings, CT with intravenous contrast is essential not only for detecting infarction but also for excluding active extravasation or associated injuries.^[26]

Management

Conservative Approaches

Conservative management forms the cornerstone of treatment for splenic infarction, particularly in hemodynamically stable patients without complications, focusing on symptom relief and addressing precipitating factors. Supportive care includes analgesia with nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids for left upper quadrant pain, intravenous hydration to maintain perfusion, and bed rest to minimize rupture risk.^[1]^[28] Most uncomplicated cases resolve spontaneously within 7 to 14 days under this approach, with symptoms such as pain and fever typically abating without intervention.^[1]^[16] Treatment must target the underlying etiology to prevent recurrence or extension of infarction. For thromboembolic causes, such as atrial fibrillation or endocarditis, anticoagulation with low-molecular-weight heparin or warfarin (target INR 2.0-3.0) is recommended, as it improves long-term survival without increasing bleeding risk in stable patients.^[29]^[30] In cases of septic emboli, broad-spectrum intravenous antibiotics are initiated promptly, guided by blood cultures and echocardiography.^[1] For patients with sickle cell disease, supplemental oxygen and aggressive hydration correct hypoxia and acidosis, reducing further sickling and infarction progression.^[1] Close monitoring is essential, with hospitalization for initial observation in moderate to severe cases to assess for hemodynamic instability or evolving complications. Serial abdominal imaging, such as ultrasound or CT, is performed if symptoms persist beyond 48-72 hours or if large infarcts (>50% splenic involvement) are present to evaluate for abscess formation or rupture.^[28]^[30] Patients with significant splenic infarction leading to impaired splenic function (hyposplenism) should receive vaccinations against encapsulated bacteria—pneumococcal (PCV13 followed by PPSV23), meningococcal (MenACWY and MenB), and Haemophilus influenzae type b (Hib)—to mitigate overwhelming post-splenectomy infection risk, ideally administered 14 days post-diagnosis or prior to discharge on a case-by-case basis.^[31] Outpatient management is appropriate for stable patients with small, asymptomatic infarcts confirmed by imaging, involving follow-up with serial clinical assessments and specialist consultation (e.g., hematology or cardiology) within 1-2 weeks.^[30] For pain control, opioids are preferred over NSAIDs in patients with underlying coagulopathy to avoid exacerbating bleeding tendencies, and all individuals should be monitored for ileus through regular evaluation of bowel sounds and abdominal distension.^[32]^[1]

Interventional and Surgical Options

Interventional and surgical options are reserved for severe or complicated cases of splenic infarction where conservative management fails, particularly in the presence of hemodynamic instability, splenic rupture, abscess formation, or persistent symptoms beyond two weeks. These indications arise when complications such as hemorrhage, pseudocyst development, or ongoing ischemia threaten patient stability, necessitating prompt evaluation for invasive procedures to prevent further deterioration.^[1]^[28] Therapeutic embolization involves angiographic occlusion of splenic artery branches to reduce blood flow and alleviate hypersplenism-associated infarction, often employed pre- or post-infarction in patients with hematologic disorders like cirrhosis or portal hypertension. This minimally invasive technique targets segmental vessels to induce controlled infarction, preserving overall splenic function while improving cytopenias such as thrombocytopenia. Success rates exceed 85% in achieving hematologic improvement and symptom relief, with low rates of major complications when limited to 50-70% splenic infarction.^[33]^[34]^[35] Splenectomy remains the definitive surgical intervention for refractory cases, performed via open or laparoscopic approaches, with the latter preferred due to reduced morbidity, shorter hospital stays, and faster recovery. Laparoscopic splenectomy is particularly suitable for stable patients, allowing for partial resection in segmental infarcts to retain residual splenic tissue and immune function. Partial splenectomy uses techniques like ultrasonic scalpel or radiofrequency ablation to excise infarcted segments while sparing healthy parenchyma.^[28]^[36]^[28] Outcomes for splenectomy in splenic infarction vary by urgency; emergency cases for rupture or instability are associated with higher mortality, around 20%, compared to elective procedures.^[37]^[11] Advances in laparoscopic methods have reduced recovery time to 3-7 days for most patients, enabling earlier resumption of normal activities compared to open surgery's 7-14 days.^[18]^[36]^[38] Postoperative management for asplenic patients focuses on preventing overwhelming post-splenectomy infection (OPSI), which carries high mortality. Lifelong vaccination against encapsulated bacteria—including pneumococcus, Haemophilus influenzae type b, and Neisseria meningitidis—is recommended, ideally administered 2 weeks preoperatively or 2 weeks postoperatively, with annual influenza vaccination. Prophylactic antibiotics, such as penicillin, are advised for at least 1-3 years or lifelong in high-risk adults, alongside patient education on infection signs and medical alert identification.^[39]^[40]^[41]

Complications and Prognosis

Complications

Splenic infarction can lead to several local complications arising from the necrotic tissue. These include the formation of splenic abscesses, a rare complication (overall incidence of splenic abscesses approximately 0.1-0.7%) due to bacterial overgrowth in the infarcted area and often necessitating percutaneous or surgical drainage.^[42] Pseudocyst formation represents another potential issue, involving sterile fluid collections within the spleen that may require intervention if symptomatic.^[11] Hemorrhage or aneurysm development in the infarcted region can also arise, posing risks of further vascular compromise.^[1] Splenic rupture, though rare, is a life-threatening event characterized by sudden peritonitis and hemodynamic instability, typically demanding emergent splenectomy.^[18] Systemic complications may manifest as sepsis, particularly when infarcted tissue becomes a nidus for bacterial proliferation, such as in cases involving septic emboli.^[28] Portal vein thrombosis is another associated risk, potentially extending from the splenic vein involvement and leading to broader mesenteric vascular issues if untreated.^[1] In patients undergoing splenectomy for severe infarction, post-operative risks include overwhelming post-splenectomy infection (OPSI), a fulminant bacterial sepsis with a mortality rate of 50-70% if it develops, though its lifetime incidence is low at 0.1-0.5%.^[43] Additionally, splenectomy elevates the risk of thrombosis, including portal vein events, a serious complication with potential for high morbidity if untreated.^[43] Chronic sequelae encompass splenic atrophy, where repeated or extensive infarctions lead to fibrosis and functional loss, as seen in conditions like sickle cell disease.^[44] Recurrence of hypersplenism may occur if only partial splenic preservation is achieved during management.^[1] The overall incidence of these complications is estimated at around 20%, but it rises significantly in massive infarcts involving more than 50% of the spleen or with delayed diagnosis, increasing the likelihood of secondary events like abscess or rupture.^[45]^[1]

Prognosis

The prognosis of splenic infarction is generally favorable in uncomplicated cases managed conservatively, with 70-80% of patients experiencing a benign course characterized by resolution of symptoms within 7-14 days through supportive care such as hydration and analgesics.^[1] For isolated splenic infarctions without underlying severe conditions, mortality rates are low, typically under 5%, though overall in-hospital mortality rates reported in literature range from 5% to 34% depending on comorbidities.^[30]^[6] However, outcomes worsen significantly in cases associated with underlying malignancy or massive infarction involving more than 50% of the splenic parenchyma, where mortality can rise to 20-35%, often due to rapid progression and multiorgan involvement.^[46]^[18] Prognosis varies markedly by etiology; traumatic or embolic causes treated promptly with embolization or anticoagulation achieve excellent resolution rates exceeding 95%, with low recurrence if the underlying trigger is addressed.^[1] In contrast, hematologic disorders such as leukemia or myeloproliferative neoplasms yield poorer long-term survival, largely dictated by the primary disease progression rather than the infarction itself.^[18]^[47] Key factors influencing recovery include infarct size, patient age, and comorbidities; small infarcts affecting less than 25% of the spleen often lead to full functional recovery without sequelae, whereas extensive involvement greater than 50% increases complication risks and prolongs hospital stays.^[16]^[18] Patients over 60 years old or those with significant comorbidities, such as renal failure, face heightened mortality risks, with 30-day rates up to 23% in emergency settings. Recent multicenter studies as of 2024 identify high triage acuity, uremia requiring renal replacement therapy, and active malignancy as key independent risk factors for mortality.^[48]^[6]^[6] Following splenectomy for severe cases, asplenic patients carry an annual risk of overwhelming post-splenectomy infection (OPSI) of approximately 0.4-1%, with lifetime risks up to 5%; prophylactic vaccinations and regular follow-up can substantially mitigate this and reduce overall mortality.^[49]^[40] Recent studies from 2021-2025 highlight improved outcomes through early imaging and targeted embolization, lowering complication rates in non-COVID cases, though COVID-19-associated infarctions are linked to hypercoagulability and potentially worse outcomes.^[50]^[7] Complications such as abscess formation or rupture can further impair survival if not addressed promptly.^[1]

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[48]
Anticoagulant Therapy Is Associated With Decreased Long-Term ...
Background: Patients with splenic infarction (SI) are associated with a prothrombotic state and are vulnerable to subsequent thromboembolic complications.